Abstract
In the present study, the protective effects of 10% ethanol extract of Capsosiphon fulvescens (CFE10) against alcoholic liver damage were investigated in vitro using CYP2E1-overexpressing hepatocytes (HepG2/2E1). To determine whether CFE10 attenuated ethanol-induced cell death, we compared the viability of HepG2/2E1 cells treated with 250 mM ethanol in the presence or absence of CFE10. Cell viability significantly increased after treatment with CFE10 and ethanol compared with that of cells treated with only ethanol. Additionally, CFE10 inhibited ethanol-induced ROS formation and lipid peroxidation. We also found that CFE10 attenuated the mRNA expression of CYP2E1, as well as decreased ethanol-induced lipid droplets, through stimulation of the AMPK pathway. Based on these results, the protective effect of CFE10 extract from C. fulvescens against liver damage and fatty liver induced by ethanol may occur via the alleviation of oxidative stress.
Highlights
IntroductionIngested alcohol (ethanol) is absorbed from the stomach and small intestine
Ingested alcohol is absorbed from the stomach and small intestine
superoxide dismutase (SOD) activity was assayed by the method of McCord and Fridovich (1969) [15], CAT activity was determined as described by Aebi (1984) [16], hepatic glutathione-S-transferase (GST) activity was assayed according to the method of Habig and Jakoby (1981) [17], glutathione peroxidase (GPx) activity was estimated by the method of Pagila and Valentine (1967) [18], and glutathione reductase (GR) activity was measured using an adaptation of the method of Calberg and Mannervik (1975) [19]
Summary
Ingested alcohol (ethanol) is absorbed from the stomach and small intestine As it cannot be stored in the body, it is subsequently oxidized in the liver [1]. CYP2E1 has been shown to be upregulated by a chronic or excessive alcohol intake and is a major factor in oxidative stress and liver injury via the generation of ROS. Chronic or excessive alcohol consumption can induce the overproduction of ROS, which destroys the antioxidant defense systems and leads to oxidative stress in the liver [2,3,4]. We investigated the hepatoprotective effects of 10% ethanol extract from C. fulvescens against ethanol-induced oxidative stress in HepG2 cells overexpressing CYP2E1 (HepG2/2E1). The cytotoxicity was expressed as a percentage relative to the control wells, which contained no sample
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